Irazoqui JE (2014) Cell Host Microbe "DAF-tly depart stinky situations with elegans."

Irazoqui JE

[Cell Host Microbe, 2014]

During acute infection our behavior tends to change. Despite how common sickness behavior is, its molecular basis is not well understood. In a study published in Cell, Kim and colleagues (Meisel etal., 2014) implicate bacterial secondary metabolites as triggers of neural TGF-? signaling, which results in behavioral change during infection.

Vader G et al. (2014) Dev Cell "HORMA domains at the heart of meiotic chromosome dynamics."

Musacchio A, Vader G

[Dev Cell, 2014]

HORMA domain proteins are required for the careful orchestration of chromosomal organization during meiosis. Kim et al. (2014) and Silva et al. (2014) now provide structural and functional insights into the roles of C. elegans HORMA proteins, revealing parallels to the function of the HORMA protein MAD2 in mitotic checkpoint signaling.

Ma L et al. (2020) J Cell Biol "Membrane fusion drives pronuclear meeting in the one-cell embryo."

Starr DA, Ma L

[J Cell Biol, 2020]

The mechanisms that control how the two parental pronuclei fuse in the first mitosis of the embryo are poorly understood. In this issue, Rahman et al. (2020. J. Cell Biol.https://doi.org/10.1083/jcb.201909137) found that membrane fusion between pronuclear envelopes, followed by fenestration, promotes pronuclear fusion.

Kumsta C et al. (2019) J Cell Biol "Getting under the skin: Cuticle damage elicits systemic autophagy response in C. elegans."

Hansen M, Kumsta C

[J Cell Biol, 2019]

In this issue, Zhang et al. (2019. <i>J. Cell. Biol.</i> https://doi.org/10.1083/jcb.201907196) describe a molecular mechanism by which cuticular damage in the nematode <i>C. elegans</i> leads to systemic induction of autophagy by signals propagated from sensory neurons via the TGF- signaling pathway.

Hickson GRX (2022) J Cell Biol "A back-up source of microtubules for the midbody during cytokinesis."

Hickson GRX

[J Cell Biol, 2022]

During cytokinesis, microtubules become compacted into a dense midbody prior to abscission. Using genetic perturbations and imaging of C. elegans zygotes, Hirsch et al. (2022. J. Cell Biol.https://doi.org/10.1083/jcb.202011085) uncover an unexpected source of microtubules that can populate the midbody when central spindle microtubules are missing.

Little P (1992) Nature "DNA sequencing. The worm turns and delivers."

Little P

[Nature, 1992]

Supporters of large DNA sequencing projects will take heart (and find much to learn) from the report by J. Sulston and colleagues that appears on page 37 of this issue. Sulston et al. describe the first results of the Caenorhabditis elegans genome sequencing project, and have come up with not only hitherto unknown genes but also with fresh and biologically relevant information.

Labouesse M (2015) Dev Cell "Adhesion with a Sumo."

Labouesse M

[Dev Cell, 2015]

Adherens junctions (AJs) play a crucial role in epithelial tissue development and tumorigenesis, and the mechanisms controlling their assembly and disassembly have therefore attracted considerable attention. A paper from Tsur et al. (2015) in this issue of Developmental Cell now shows how sumoylation and desumoylation of E-cadherin promotes its recruitment to AJs.

Storelli G et al. (2013) Cell Metab "Metformin, microbes, and aging."

Leulier M, Storelli G, Tefit M

[Cell Metab, 2013]

The mechanisms underlying the biological activity of metformin, a widely prescribed drug to treat type 2 diabetes, remain elusive. In a recent issue of Cell, Cabreiro et al. report that in C. elegans, metformin indirectly impacts lifespan by altering the methionine metabolism of its microbial partner E. coli (Cabreiro et al., 2013).

Nguyen TP et al. (2012) BMC Biol "Folate status of gut microbiome affects Caenorhabditis elegans lifespan."

Clarke CF, Nguyen TP

[BMC Biol, 2012]

In a paper in BMC Biology Virk et al. show that Caenorhabditis elegans lifespan is extended in response to a diet of folate-deficient Escherichia coli. The deficiencies in folate biosynthesis were due to an aroD mutation, or treatment of E. coli with sulfa drugs, which are mimics of the folate precursor para-aminobenzoic acid. This study suggests that pharmacological manipulation of the gut microbiome folate status may be a viable approach to slow animal aging, and raises questions about folate supplementation.

Garsin DA et al. (2013) Gut Microbes "Candida albicans and Enterococcus faecalis in the gut: synergy in commensalism?"

Garsin DA, Lorenz MC

[Gut Microbes, 2013]

The fungus Candida albicans and the gram-positive bacterium Enterococcus faecalis are both normal residents of the human gut microbiome and cause opportunistic disseminated infections in immunocompromised individuals. Using a nematode infection model, we recently showed that co-infection resulted in less pathology and less mortality than infection with either species alone and this was partly explained by an interkingdom signaling event in which a bacterial-derived product inhibits hyphal morphogenesis of C. albicans. In this addendum we discuss these findings in the contest of other described bacterial-fungal interactions and recent data suggesting a potentially synergistic relationship between these two species in the mouse gut as well. We suggest that E. faecalis and C. albicans promote a mutually beneficial association with the host, in effect choosing a commensal lifestyle over a pathogenic one.